In:
Journal of the Renin-Angiotensin-Aldosterone System, Hindawi Limited, Vol. 18, No. 1 ( 2017-01), p. 147032031769884-
Abstract:
Unstable angina is associated with an acute systemic inflammatory reaction and circulating T lymphocytes are activated. We investigated whether in unstable angina with marked immune system activation a selective upregulation of the circulating T-cell renin–angiotensin system, modulated by angiotensin II, could occur. Methods: We studied 13 unstable angina patients, 10 patients with stable angina and 10 healthy subjects. After T-lymphocyte isolation, mRNAs for angiotensin-converting enzyme (ACE) and angiotensin type 1 receptor (AT1-R) were quantified at baseline and after angiotensin II stimulation. ACE activity in cell pellet and supernatant and angiotensin II cell content were measured. Results: Plasma renin activity was similar in controls, stable and unstable angina patients. At baseline ACE and AT1-R mRNA levels were higher ( P 〈 0.05) in T cells from unstable angina patients than in T cells from stable angina patients and controls, and further increased after angiotensin II addition to cultured T cells. ACE activity of unstable angina T cells was significantly higher than that of T cells from controls and stable angina patients. Only in T cells from unstable angina patients did angiotensin II stimulation cause the almost complete release of ACE activity in the supernatant. Conclusions: The circulating T-cell-based renin–angiotensin system from unstable angina patients was selectively upregulated. In vivo unstable angina T cells could locally increase angiotensin II concentration in tissues where they migrate independently of the circulating renin–angiotensin system.
Type of Medium:
Online Resource
ISSN:
1470-3203
,
1752-8976
DOI:
10.1177/1470320317698849
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2017
detail.hit.zdb_id:
2261873-9
